Nerve regeneration by interferon intervention in aging brain

Abstract Neural stem cells (NSCs) are shielded from viral infection by interferon (IFN) defense. As individuals age, activation of NSC decreases with a significant decline of stemness marker Sex‐determining region Y box 2 (Sox2) while IFN signaling enhances (Kalamakis et al, 2019). Given that low‐le...

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Main Authors: Fanwen Wang, Duanqing Pei
Format: Article
Language:English
Published: Springer Nature 2023-03-01
Series:EMBO Molecular Medicine
Online Access:https://doi.org/10.15252/emmm.202217307
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author Fanwen Wang
Duanqing Pei
author_facet Fanwen Wang
Duanqing Pei
author_sort Fanwen Wang
collection DOAJ
description Abstract Neural stem cells (NSCs) are shielded from viral infection by interferon (IFN) defense. As individuals age, activation of NSC decreases with a significant decline of stemness marker Sex‐determining region Y box 2 (Sox2) while IFN signaling enhances (Kalamakis et al, 2019). Given that low‐level type‐I IFN under normal physiological conditions can promote dormant hematopoietic stem cell differentiation (Baldridge et al, 2010), whether there is an inner connection between IFN signaling and NSC function remains elusive. In this issue of EMBO Molecular Medicine, Carvajal Ibanez et al (2023) reveal that IFN‐β, a type‐I interferon, induces cell‐type‐specific interferon‐stimulated genes (ISGs) and regulates global protein synthesis by orchestrating mTOR1 activity and stem cell cycle that retain NSCs at the G0 phase and repress Sox2 expression. As a consequence, NSCs exit the activation state and become inclined to differentiation.
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spelling doaj-art-e98fc2f0d4e34fa8a1ffb9c2569c45882025-08-20T03:05:53ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842023-03-011541310.15252/emmm.202217307Nerve regeneration by interferon intervention in aging brainFanwen Wang0Duanqing Pei1Laboratory of Cell Fate Control, School of Life Sciences, Westlake UniversityLaboratory of Cell Fate Control, School of Life Sciences, Westlake UniversityAbstract Neural stem cells (NSCs) are shielded from viral infection by interferon (IFN) defense. As individuals age, activation of NSC decreases with a significant decline of stemness marker Sex‐determining region Y box 2 (Sox2) while IFN signaling enhances (Kalamakis et al, 2019). Given that low‐level type‐I IFN under normal physiological conditions can promote dormant hematopoietic stem cell differentiation (Baldridge et al, 2010), whether there is an inner connection between IFN signaling and NSC function remains elusive. In this issue of EMBO Molecular Medicine, Carvajal Ibanez et al (2023) reveal that IFN‐β, a type‐I interferon, induces cell‐type‐specific interferon‐stimulated genes (ISGs) and regulates global protein synthesis by orchestrating mTOR1 activity and stem cell cycle that retain NSCs at the G0 phase and repress Sox2 expression. As a consequence, NSCs exit the activation state and become inclined to differentiation.https://doi.org/10.15252/emmm.202217307
spellingShingle Fanwen Wang
Duanqing Pei
Nerve regeneration by interferon intervention in aging brain
EMBO Molecular Medicine
title Nerve regeneration by interferon intervention in aging brain
title_full Nerve regeneration by interferon intervention in aging brain
title_fullStr Nerve regeneration by interferon intervention in aging brain
title_full_unstemmed Nerve regeneration by interferon intervention in aging brain
title_short Nerve regeneration by interferon intervention in aging brain
title_sort nerve regeneration by interferon intervention in aging brain
url https://doi.org/10.15252/emmm.202217307
work_keys_str_mv AT fanwenwang nerveregenerationbyinterferoninterventioninagingbrain
AT duanqingpei nerveregenerationbyinterferoninterventioninagingbrain